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accession-icon GSE11045
Expression data from kidney and liver
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

mRNA expression differences between the liver and kidney of an adult male (homo sapien) were investigated using three technical replicates.

Publication Title

RNA-seq: an assessment of technical reproducibility and comparison with gene expression arrays.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE34900
RET fusion genes, BCR-RET and FGFR1OP-RET, are associated with chronic myelomonocytic leukemia, display sensitivity to Sorafenib, an inhibitor of tyrosine-kinase activity and enhance monocytic differentiation
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Myeloproliferative neoplasms are frequently associated with aberrant constitutive tyrosine kinase (TK) activity resulting from point mutations or chimaeric fusion genes, such as BCR ABL1 or JAK2 V617F. We report here for the first time in hematological malignancies, two novel fusion genes involving the TK RET, BCR-RET and FGFR1OP-RET, in chronic myelo monocytic leukemia (CMML) cases. The two RET fusion genes lead to the aberrant activation of RET, are able to transform hematopoietic cells and skew the hematopoietic differentiation program towards the monocytic/macrophage lineage. We also report that the BCR-RET fusion protein is insensitive to Imatinib but sensitive to Sorafenib in vivo. CMML is an hematopoietic malignancy associated with the frequent activation of the RAS pathway. The RET fusion genes seems to constitutively mimic the same signaling pathway than RAS mutations. Overall, the RET fusion genes behaviors in the monocytic lineage underlie the role of the normal RET TK activity during the physiological monocytic differentiation.

Publication Title

RET fusion genes are associated with chronic myelomonocytic leukemia and enhance monocytic differentiation.

Sample Metadata Fields

Cell line

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accession-icon GSE13344
Exon Array expression data from 13 areas of the late second trimester human brain
  • organism-icon Homo sapiens
  • sample-icon 186 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Tissue was microdissected from 13 regions, including 9 distinct neocortical areas, from both left and right sides of four late second trimester human brain specimens. Gene- and exon-level differential expression analyses were performed by mixed model, nested analysis of variance using the XRAY software from Biotique Systems. Further details available in Johnson, Kawasawa, et al., "Functional and Evolutionary Insights into Human Brain Development through Global Transcriptome Analysis" Neuron, Volume 62, Issue 4, 2009

Publication Title

Functional and evolutionary insights into human brain development through global transcriptome analysis.

Sample Metadata Fields

Age

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accession-icon SRP187302
Slow transcriptional elongation causes embryonic lethality and perturbs kinetic coupling of long neural genes [4sURDB-Seq]
  • organism-icon Mus musculus
  • sample-icon 41 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

The rate of RNA Polymerase II (RNAPII) elongation has an important role in the control of Alternative splicing (AS); however, the in vivo consequences of an altered elongation rate are unknown. Here, we generated mouse embryonic stem cells (ESCs) knocked-in for a slow elongating form of RNAPII. We show that a reduced transcriptional elongation rate results in early embryonic lethality in mice and impairs the differentiation of ESCs into the neural lineage. This is accompanied by changes in splicing and in gene expression in ESCs and along the pathway of neuronal differentiation. In particular, we found a crucial role for RNAPII elongation rate in transcription and splicing of long neuronal genes involved in synapse signaling. The impact of the kinetic coupling of RNAPII elongation rate with AS is more predominant in ESC-differentiated neurons than in pluripotent cells. Our results demonstrate the requirement for an appropriate transcriptional elongation rate to ensure proper gene expression and to regulate AS during development. Overall design: 4sURDB-Seq mouse wt and homozygous Polr2a[R749H] mutant embryonic stem cells in triplicates.

Publication Title

A slow transcription rate causes embryonic lethality and perturbs kinetic coupling of neuronal genes.

Sample Metadata Fields

Treatment, Subject

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accession-icon SRP148569
Impact of Escherichia coli K12 and O18 on human platelets: effects on platelet activation, spliced platelet RNAs and proteins
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We report RNA-sequencing data of 12 platelet samples isolated from four healthy individuals and incubated with either E. coli K12, E. coli O18 or no bacteria. This dataset highlights the differential effect of bacteria on spliced platelet RNA profiles. Overall design: Blood platelets were isolated from whole blood in citrate-coated BD Vacutainers by standard centrifugation and multiple washing steps. Total RNA was extracted from the platelet pellet, subjected to cDNA synthesis and SMARTer amplification, fragmented by Covaris shearing, and prepared for sequencing using the TruSeq Nano DNA Sample Preparation Kit. Subsequently, pooled sample libraries were sequenced on the Illumina HiSeq 2500 platform. All steps were quality-controlled using Bioanalyzer 2100 with RNA 6000 Picochip, DNA 7500 and DNA High Sensitivity chips measurements. For further downstream analyses, reads were quality-controlled using Trimmomatic, mapped to the human reference genome using STAR, and intron-spanning reads were summarized using HTseq.

Publication Title

Impact of Escherichia coli K12 and O18:K1 on human platelets: Differential effects on platelet activation, RNAs and proteins.

Sample Metadata Fields

Specimen part, Disease, Subject

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accession-icon GSE76794
Gene profiling of primary chicken embryo fibroblasts (CEFs) grown under the conditions of contact-inhibition, serum starvation, or both in comparison to normal cycling cells
  • organism-icon Gallus gallus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

To investigate the differences of expression patterns in primary chicken embryo fibroblasts (CEFs) under conditions of contact-inhibition and serum starvation, we undertook a gene profiling study to characterize the transcriptomes of CEFs grown under conditions of contact inhibition, serum starvation or both, in relation to normal growing (cycling) cells.

Publication Title

Extracellular Signal-Regulated Kinase 2 and CHOP Restrict the Expression of the Growth Arrest-Specific p20K Lipocalin Gene to G0.

Sample Metadata Fields

Specimen part

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accession-icon GSE70421
SMARCB1-deficient rhaboid tumors of the kidney and renal medullary carcinomas.
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to compared gene expression profilings in various tumors of the kidney.

Publication Title

Balanced Translocations Disrupting SMARCB1 Are Hallmark Recurrent Genetic Alterations in Renal Medullary Carcinomas.

Sample Metadata Fields

Specimen part

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accession-icon GSE25300
Hypermethylation of miR-34b is associated with CREB overexpression and Myeloid Cell Transformation
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Increased CREB levels and upregulation of its target genes expression resulted in increased myelopoiesis and colony formation.

Publication Title

MicroRNA-34b promoter hypermethylation induces CREB overexpression and contributes to myeloid transformation.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

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accession-icon GSE49093
The ETS family member GABPa mediates the development of castrate-resistant prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The ETS family member GABPα modulates androgen receptor signalling and mediates an aggressive phenotype in prostate cancer.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE49083
The ETS family member GABPa mediates the development of castrate-resistant prostate cancer (BeadChip)
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

In prostate cancer, the androgen receptor (AR) is a key transcription factor at all disease stages. We recently showed that during progression to castrate-resistant prostate cancer the AR acquires the ability to bind to a distinct set of genomic sites in tissue samples and that some of the genes that are regulated by the AR in these conditions correlate with poor prognosis. Based on this work we hypothesised that the AR is reprogrammed through interactions with other transcription factors. In the present study we show that GABP, an ETS transcription factor which is upregulated in CRPC, is an AR-interacting transcription factor. Ectopic expression of GABPA in prostate cancer cell-lines enables them to acquire some of the molecular and cellular characteristics of CRPC tissues as well as more aggressive growth phenotypes.

Publication Title

The ETS family member GABPα modulates androgen receptor signalling and mediates an aggressive phenotype in prostate cancer.

Sample Metadata Fields

Cell line, Treatment

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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